Abstract
Introduction: Klebsiella pneumoniae is one of the etiological factors of nosocomial infections. Recently, infections caused by these bacteria have become more dangerous due to the acquired resistance to many antibiotics, severely limiting therapeutic options. The most common mechanism of resistance in K. pneumoniae rods is the production of extended-spectrum β-lactamases (ESBL). However, a more perilous mechanism is the production of carbapenemases. The course of the infection process is also influenced by various virulence characteristics, primarily enabling adhesion and aiding in avoiding host immune responses. Most genes encoding mechanisms of resistance and virulence are located on plasmids, facilitating their spread. The aim of the study was to detect selected virulence genes among clinical multidrug-resistant strains of K. pneumoniae.
Materials and methods: We determined the drug susceptibility of strains and confirmed the presence of antibiotic resistance mechanisms using phenotypic methods. Additionally, we assessed the presence of genes encoding selected resistance mechanisms and genes determining selected virulence factors. A total of 134 strains from various hospital units were used for the study.
Results: The highest percentage of strains was isolated from urine (46%). Among the isolates, 72% were from male patients. Fifty-seven percent of K. pneumoniae produced ESBL (KpESBL), while the remaining 43% carried the New Delhi metallo-β- lactamase (NDM) mechanism. The drug susceptibility of the KpESBL varied, with full sensitivity observed only in the case of antibiotics from the carbapenem group. New Delhi metallo- β-lactamase-producing K. pneumoniae showed sensitivity only to amikacin and gentamicin. In KpESBL strains, genes from the TEM family were most observed (74/76). Most of the strains had all 4 β-lactamase-encoding genes (61/76). In the group of strains producing carbapenemases, only the bla NDM gene was detected. Regardless of the resistance mechanisms, the tested strains most often had virulence genes related to the adhesion ability (fimH) and the structure of LPS (wabG).